ライフサイエンスコーパス: sLe(X)

1 mon resonance experiments determined that an sLe(X) analogue (TBC1269) competitively inhibited, via s

2 tennary N-glycans, and 3) reduced LacNAc and sLe(X) on N-glycans and on core 2 O-glycans.

3 tin ligand expression and related LacNAc and sLe(X) structures, MALDI-TOF and MALDI-TOF/TOF mass spec

4 Based on anti-sLe(X) antibody and lectin probing experiments on 4-F-Gl

5 Unlike anti-sLe(X) mAbs, CHO-131 binding also indicates C2GnT activi

6 These results indicate that P-selectin binds sLeX in a shallow cleft that is similar to the mannose-b

7 nal N-acetylglucosamine residue also blocked sLe(X) formation in cells.

8 een implicated in P-selectin binding to both sLeX and 3-sulfated galactosylceramide (sulfatide).

9 man RBCs showed dose-dependent inhibition by sLeX.

10 n wall shear stress within the flow chamber, sLe(X)/aICAM-1 microsphere site density, and P-selectin/

11 inguished by the mAb HECA-452, which detects sLe(X)-related glycans.

12 sion on P-selectin, only peptides expressing sLe(X) groups showed rolling adhesion on E-selectin.

13 Although all peptides expressing sLe(X), tyr-SO(3), or both supported some form of rollin

14 Similar binding kinetics are expected for sLe(X)-selectin interactions.

15 emolytic activity and a reduced affinity for sLeX.

16 The lectin domain responsible for sLeX binding is in domain 4 of Ply, which contains candi

17 lectin-carbohydrate binding specificity from sLeX to oligomannose.

18 eu5Acalpha2-3Galbeta1-4(Fucalpha1-3) GlcNAc; sLe(X)) in tumor cells.

19 ycans released from 4-F-GlcNAc-treated human sLe(X) (+) T cells and leukemic KG1a cells.

20 if this oligosaccharide lacked fucose or if sLe(X) was extended from a core 1 branch.

21 ermediate for downstream enzymes involved in sLe(X) assembly, and (iii) generation of several glycans

22 The last step in sLe(X) biosynthesis is the alpha1,3-fucosyltrasferase (F

23 e acetylated form of this compound inhibited sLe(X) formation in U937 monocytic leukemia cells, sugge

24 t was hypothesized that 4-F-GlcNAc inhibited sLe(X) formation by incorporating into LacNAc and blocki

25 sialyllactosaminyl glycans convertible into sLe(X) are abundantly expressed on human monocytes yet a

26 tyrosine sulfation (GP1), and one that lacks sLe(X) but has three N-terminal tyr-SO(3) groups (SP3).

27 lectin domain that binds the sialyl LewisX (sLeX) carbohydrate (Neu5Acalpha2-3Galbeta1-4(Fucalpha1-3

28 the highest affinity for the sialyl LewisX (sLeX) structure, with a K(d) of 1.88 x 10(-5) M.

29 -5T-Fuc, that blocks FUT activity and limits sLe(X) presentation on HepG2 cells with an EC(50) in the

30 the consequences of inhibiting FUT-mediated sLe(X) formation.

31 a useful probe that can be used to modulate sLe(X) levels in cells to evaluate the consequences of i

32 The C2-O-sLe(X) motif occurs primarily on sialomucins and has bee

33 o sLe(X) extended from a core 2 branch (C2-O-sLe(X)), but CHO-131 demonstrated no reactivity if this

34 on the disaccharides diverts the assembly of sLe(X) from endogenous cell surface glycoconjugates.

35 ring strategy to inhibit the biosynthesis of sLe(X) in cancer cells using peracetylated 5-thio-L-fuco

36 lycosyltransferases that regulate display of sLe(X) reveal high transcript levels among circulating m

37 ethanol (AcGnG-NM) reduces the expression of sLe(X) and diminishes binding in vitro to selectin-coate

38 The reduction of sLe(X) by the 4'-deoxy analog also diminished experiment

39 Yet, regulation of sLe(X) and related E-selectin ligand expression in PCa c

40 These compounds represent a novel series of sLe(X) mimetics with antiinflammatory activity.

41 iver-metastatic PCa and dictate synthesis of sLe(X) and E-selectin ligands on metastatic PCa cells.

42 tins with low affinity comparable to that of sLe(X)-selectin interactions.

43 in P-selectin binding to either sulfatide or sLeX.

44 distinct PSGL-1 peptides: one that possesses sLe(X) in conjunction with three N-terminal tyr-SO(3) gr

45 tyr-SO(3) groups (SGP3), one that possesses sLe(X) without tyrosine sulfation (GP1), and one that la

46 Monocytes prominently present sLe(X) decorations on an array of protein scaffolds, inc

47 Separately, sLe(X)/P-selectin interactions support rolling and aICAM

48 tant role during selectin recognition, since sLe(X) and sialyl Lewis-a (sLe(a)) were approximately 5-

49 ctin binding at 30-100-fold lower doses than sLe(X).

50 Such analysis predicts that sLe(X) expression varies directly with sialyltransferase

51 Our results show that sLe(X)/aICAM-1 microspheres will firmly adhere to P-sele

52 Results demonstrate that 1) the sLe(X) (sialyl-Lewis-X) epitope is expressed in P-select

53 s demonstrate an almost complete loss of the sLe(X) epitope on both leukocyte N- and O-glycans.

54 hat mediate the binding of P-selectin to the sLeX carbohydrate have been determined.

55 s showed that blocking binding of Ply to the sLeX glycolipid on RBCs prevents deposition of the toxin

56 archetypal CDC requires interaction with the sLeX glycolipid cellular receptor as an essential step b

57 CHO-131 bound to sLe(X) extended from a core 2 branch (C2-O-sLe(X)), but

58 3) The activity of enzymes contributing to sLe(X) formation in leukocytes likely varies as ST3[Galb

59 the assembly of oligosaccharides related to sLe(X) synthesis, and the assembly of oligosaccharides o

60 ii) generation of several glycans related to sLe(X).

61 f aICAM-1/ICAM-1 interaction is greater when sLe(X)/P-selectin interactions are present.

62 e-sulfated, in addition to glycosylated with sLe(X), to successfully interact with P-selectin.

63 We show that P-selectin's interaction with sLe(X) mechanistically facilitates firm adhesion mediate

64 Thus, interfering with sLe(X) assembly might provide a chemotherapeutic method

65 selectin binding determinant sialyl Lewis X (sLe(X)) and display markedly greater adhesive interactio

66 2 O-glycans terminated with sialyl-Lewis x (sLe(X)) are functionally important oligosaccharides that

67 Sialyl-Lewis X (sLe(X)) is a tetrasaccharide that serves as a ligand for

68 Sialyl Lewis X (sLe(X)) on prostate cancer (PCa) cells is thought to pro

69 Clustered presentation of sialyl Lewis X (sLe(X)) on tumor cell mucins is thought to facilitate me

70 -acetyllactosamine (LacNAc), sialyl Lewis X (sLe(X)), and related lectin ligands on effector leukocyt

71 P- and L-selectin binding to sialyl Lewis X (sLe(X))-containing ligands, and the myosin-actin motor p

72 le oligosaccharides based on sialyl Lewis-X (sLe(X)) and complex molecules with the core-2 structure

73 (Galbeta1,4GlcNAc) to create sialyl Lewis-X (sLe(X)) and related sialofucosylated glycans on human le

74 ate the presence of both the sialyl Lewis-X (sLe(X)) and the di-sialylated T-antigen (NeuAcalpha2,3Ga

75 pate in the formation of the sialyl Lewis-X (sLe(X)) epitope on O-glycans linked to a leukocyte cell-

76 bonds in the pentasaccharide sialyl Lewis-X (sLe(X)-5) between 5 and 37 degrees C in water.

77 d with the selectin ligand, sialyl Lewis(X) (sLe(X)), and an antibody against ICAM-1, aICAM-1, are pe

78 pies of the tetrasaccharide sialyl-Lewis(x) (sLe(X)), as well as a cluster of three tyrosine sulfate